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Background: Several randomized studies have shown that the combination of programmed cell death 1 (PD-1) inhibitor and chemotherapy is efficacious as a treatment for advanced non-small-cell lung cancer (NSCLC). However, in the neoadjuvant setting, there is scarce evidence of the effectiveness and safety of the combinations in squamous NSCLC. We conducted a retrospective study to evaluate neoadjuvant PD-1 inhibitor plus chemotherapy in resectable squamous NSCLC. Methods: Patients from Beijing Chest Hospital, Capital Medical University, between October 2019 and October 2021, treated with PD-1 inhibitors and chemotherapy for resectable squamous NSCLC were retrospectively studied. The primary objectives were to assess the pathological tumor response and safety of neoadjuvant PD-1 inhibitors and chemotherapy. Results: 63 patients with resectable squamous NSCLC stage IIA-IIIB were included. Two to four cycles of PD-1 inhibitors (37 cases with camrelizumab, 11 cases with toripalimab, 8 cases with tislelizumab, and 7 cases with sintilimab) and chemotherapy were administered prior to surgery. 42 patients (66.7%) achieved a major pathologic response (MPR), including 25 (39.7%) with a pathologic complete response (pCR). Twenty-one patients (33.3%) experienced grade 3 neoadjuvant treatment-related adverse events (TRAEs), and no patient had grade 4 or 5 TRAE. Conclusion: Neoadjuvant PD-1 inhibitors and chemotherapy are feasible therapies for resectable squamous NSCLC. It was associated with a 66.7% MPR rate, 39.7% pCR rate, and tolerable toxicity.

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We employed a previously described procedure, based on circular dichroism (CD) spectroscopy, to quantify the distribution of conformational states adopted by equimolar mixtures of complementary G-rich and C-rich DNA strands from the promoter regions of the VEGF and Bcl-2 oncogenes. Spectra were recorded at different pHs, concentrations of KCl, and temperatures. The temperature dependences of the fractional populations of the duplex, G-quadruplex, i-motif, and coiled conformations of each promoter were then analyzed within the framework of a thermodynamic model to obtain the enthalpy and melting temperature of each folded-to-unfolded transition involved in the equilibrium. A comparison of the conformational data on the VEGF and Bcl-2 DNA with similar results on the c-MYC DNA, which we reported previously, reveals that the distribution of conformational states depends on the specific DNA sequence and is modulated by environmental factors. Under the physiological conditions of room temperature, neutral pH, and elevated concentrations of potassium ions, the duplex conformation coexists with the G-quadruplex conformation in proportions that depend on the sequence. This observed conformational diversity has biological implications, and it further supports our previously proposed thermodynamic hypothesis of gene regulation. In that hypothesis, a specific distribution of duplex and tetraplex conformations in a promoter region is fine-tuned to maintain the healthy level of gene expression. Any deviation from a healthy distribution of conformational states may result in pathology stemming from up- or downregulation of the gene.

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BACKGROUND: Preliminary researches conformed that neoadjuvant immunotherapy combined with chemotherapy had a significant short-term effect in resectable non-small cell lung cancer (NSCLC), but there were few clinical trials about neoadjuvant chemoimmunotherapy in China. We aimed to assess retrospectively the antitumour activity and safety of neoadjuvant chemoimmunotherapy for resectable stage Ib-IIIb NSCLC. METHODS: Twenty patients who had been diagnosed as stage Ib-IIIb NSCLC and received chemoimmunotherapy as neoadjuvant treatment between November 2019 and December 2020, in Beijing Chest Hospital, Capital Medical University were recruited. These patients received neoadjuvant treatment for 21 days as a cycle and antitumour activity and safety were evaluated every two cycles. RESULTS: Of 20 patients received neoadjuvant chemoimmunotherapy, 17 patients underwent surgical resection. 16 patients had R0 resection (no residual tumor resection) and 1 patient had R1 resection (microscopic residual tumor resection). Radiographic objective response rate (ORR) was 85.0% (4 complete response, 13 partial response). 5.0% (1/20) of patients had stable disease, and 10.0% (2/20) of patients had progression disease. The major pathologic response (MPR) was 47.1% (8/17), and complete pathologic response (CPR) was 29.4% (5/17). 1 case developed grade IV immune-related pneumonia (IRP) and 9 (45.0%) cases had grade III hematologic toxicity. CONCLUSIONS: Immunotherapy combined with chemotherapy as neoadjuvant therapy has a better efficiency and tolerable adverse effects for patients with resectable NSCLC in stage Ib-IIIb.

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BACKGROUND: The butyrophilin (BTN) family has many members with diverse functions related to immunomodulation, initiation and progression of tumors. BTN3A3 belongs to the BTN family, and exploring its expression and correlation with the prognosis of non-small cell lung cancer (NSCLC) patients has great clinical significance. METHODS: Clinical specimens were used to detect BTN3A3 expression. Small interfering RNA (siRNA) was used to knock down BTN3A3 and analyze the proliferative, migratory and invading ability of the transfected NSCLC cells. Multiplex immunofluorescence staining was used to detect the expression of BTN3A3 protein in the tumor microenvironment (TME). We analyzed the relationship between the expression of BTN3A3 and the clinicopathological features and prognosis of NSCLC patients. RESULTS: The expression of BTN3A3 in NSCLC tissues was significantly lower than in adjacent tissues, and patients with low expression of BTN3A3 had late clinical stages and lower degree of tumor differentiation. Knocking down BTN3A3 promoted the proliferation, migration and invasion of NSCLC. In the TME, the density of BTN3A3+ tumor cells positively correlated with the density of CD8+ T cells, and the patients with low expression of BTN3A3 had poor overall survival (OS). CONCLUSIONS: Changes in the BTN3A3 expression level may play a potential key role in the carcinogenesis and development of NSCLC. Patients with low expression of BTN3A3 showed a more aggressive and invasive phenotype and a lower level of CD8+ T-cell infiltration, which may be an important factor affecting the OS of NSCLC patients.

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BACKGROUND AND AIM: Tubulointerstitial nephritis antigen-like 1 (TINAGL1), as a novel matricellular protein, has been demonstrated to participate in cancer progression, whereas the potential function of TINAGL1 in gastric cancer (GC) remains unknown. METHODS: The expression pattern of TINAGL1 in GC was examined by immunohistochemistry, ELISA, real-time polymerase chain reaction, and Western blot. Correlation between TINAGL1 and matrix metalloproteinases (MMPs) was analyzed by the GEPIA website and Kaplan-Meier plots database. The lentivirus-based TINAGL1 knockdown, CCK-8, and transwell assays were used to test the function of TINAGL1 in vitro. The role of TINAGL1 was confirmed by subcutaneous xenograft, abdominal dissemination, and lung metastasis model. Microarray experiments, ELISA, real-time polymerase chain reaction, and Western blot were used to identify molecular mechanism. RESULTS: TINAGL1 was increased in GC tumor tissues and associated with poor patient survival. Moreover, TINAGL1 significantly promoted GC cell proliferation and migration in vitro as well as facilitated GC tumor growth and metastasis in vivo. TINAGL1 expression in GC cells was accompanied with increasing MMPs including MMP2, MMP9, MMP11, MMP14, and MMP16. GEPIA database revealed that these MMPs were correlated with TINAGL1 in GC tumors and that the most highly expressed MMP was MMP2. Mechanically, TINAGL1 regulated MMP2 through the JNK signaling pathway activation. CONCLUSIONS: Our data highlight that TINAGL1 promotes GC growth and metastasis and regulates MMP2 expression, indicating that TINAGL1 may serve as a therapeutic target for GC.

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SARS-CoV-2, a ß-coronavirus, has rapidly spread across the world, highlighting its high transmissibility, but the underlying morphogenesis and pathogenesis remain poorly understood. Here, we characterize the replication dynamics, cell tropism and morphogenesis of SARS-CoV-2 in organotypic human airway epithelial (HAE) cultures. SARS-CoV-2 replicates efficiently and infects both ciliated and secretory cells in HAE cultures. In comparison, HCoV-NL63 replicates to lower titers and is only detected in ciliated cells. SARS-CoV-2 shows a similar morphogenetic process as other coronaviruses but causes plaque-like cytopathic effects in HAE cultures. Cell fusion, apoptosis, destruction of epithelium integrity, cilium shrinking and beaded changes are observed in the plaque regions. Taken together, our results provide important insights into SARS-CoV-2 cell tropism, replication and morphogenesis.

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BACKGROUND: The main cause of cancer death is lung cancer (LC) which usually presents at an advanced stage, but its early detection would increase the benefits of treatment. Blood is particularly favored in clinical research given the possibility of using it for relatively noninvasive analyses. Copy number variation (CNV) is a common genetic change in tumor genomes, and many studies have indicated that CNV-derived cell-free DNA (cfDNA) from plasma could be feasible as a biomarker for cancer diagnosis. METHODS: In this study, we determined the possibility of using chromosomal arm-level CNV from cfDNA as a biomarker for lung cancer diagnosis in a small cohort of 40 patients and 41 healthy controls. Arm-level CNV distributions were analyzed based on z score, and the machine-learning algorithm Extreme Gradient Boosting (XGBoost) was applied for cancer prediction. RESULTS: The results showed that amplifications tended to emerge on chromosomes 3q, 8q, 12p, and 7q. Deletions were frequently detected on chromosomes 22q, 3p, 5q, 16q, 10q, and 15q. Upon applying a trained XGBoost classifier, specificity and sensitivity of 100% were finally achieved in the test group (12 patients and 13 healthy controls). In addition, five-fold cross-validation proved the stability of the model. Finally, our results suggested that the integration of four arm-level CNVs and the concentration of cfDNA into the trained XGBoost classifier provides a potential method for detecting lung cancer. CONCLUSION: Our results suggested that the integration of four arm-level CNVs and the concentration from of cfDNA integrated withinto the trained XGBoost classifier could become provides a potentially method for detecting lung cancer detection. KEY POINTS: Significant findings of the study: Healthy individuals have different arm-level CNV profiles from cancer patients. Amplifications tend to emerge on chromosome 3q, 8q, 12p, 7q and deletions tend to emerge on chromosome 22q, 3p, 5q, 16q, 10q, 15q. WHAT THIS STUDY ADDS: CfDNA concentration, arm 10q, 3q, 8q, 3p, and 22q are key features for prediction. Trained XGBoost classifier is a potential method for lung cancer detection.

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Our main objective is probing the effect of methylation of CLEC14A on its expression and lung adenocarcinoma (LUAD) progression. Microarray analysis was utilized to screen out differentially downregulated genes with hypermethylation in LUAD tissues. The CLEC14A expression level was measured by western blot analysis and qRT-PCR. Methylation-specific-PCR was performed to evaluate methylation status of CLEC14A. The 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromid (MTT) assay was used to check the relation between CLEC14A expression and cell proliferation. Cell cycle, cell apoptosis, migration, and invasion were respectively detected by the flow cytometry assay, wound healing assay, and transwell assay. Tumor xenograft models were established for investigating the effect of CLEC14A on tumor formation. CLEC14A expression in LUAD tissues was impaired compared with that in adjacent tissues, and CLEC14A promoter was highly methylated in LUAD. Overexpressing CLEC14A or inhibiting the methylation level of CLEC14A in A549 and LTEP-a-2 cells impeded the duplication of LUAD cells, promoted apoptosis, attenuated cell migration, and invasion ability, and arrested cell cycle at the G0/G1 phase. Overexpression of CLEC14A inhibited tumorigenesis of LUAD cells in nude mice. The promoter of CLEC14A is methylated in LUAD, leading to downregulation of CLEC14A in LUAD. CLEC14A acts as an antitumor role in LUAD by suppressing cell proliferation, migration, invasion, promoting cell apoptosis, and reducing tumorigenicity in nude mice. Thus, the inhibition of CLEC14A methylation is a novel strategy for the clinic treatment of LUAD.

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OBJECTIVE: We aimed to detect the role of LINC00472 via regulating miR-24-3p and death effector domain-containing DNA-binding protein in lung adenocarcinoma. METHODS: Long noncoding RNA, microRNA, and messenger RNA levels were determined using reverse transcription quantitative polymerase chain reaction. The expression of death effector domain-containing DNA-binding protein was determined using Western blot assay. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay were conducted to explore the proliferation of cells. The cell apoptosis was tested by flow cytometry assay. Target relationships between miR-24-3p, death effector domain-containing DNA-binding protein, and LINC00472 were validated by dual-luciferase reporter gene assay. RESULTS: LINC00472 and death effector domain-containing DNA-binding protein were found to be underexpressed, whereas miR-24-3p was found overexpressed in lung adenocarcinoma cell lines and tissues. Both LINC00472 and death effector domain-containing DNA-binding protein can bind to miR-24-3p. Overexpression of LINC00472 led to higher death effector domain-containing DNA-binding protein level, demoting cell proliferation while promoting apoptosis. Overexpression of miR-24-3p reduced death effector domain-containing DNA-binding protein level, which facilitated cell proliferation and inhibited cell apoptosis, as well as to some extent restrained the effects of LINC00472. The high expression of miR-24-3p in tumor cells was negatively related to LINC00472 and death effector domain-containing DNA-binding protein, whereas the expression of LINC00472 and that of death effector domain-containing DNA-binding protein were positively correlated. CONCLUSION: Our findings suggested that LINC00472 contributed to the increase in lung adenocarcinoma cell apoptosis and the inhibition of proliferation via regulating miR-24-3p/ DEDD, which might provide a novel insight into potential therapeutic approach for lung adenocarcinoma.

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Myeloid-derived suppressor cells (MDSCs) are a prominent component of the pro-tumoral response. The phenotype of and mechanisms used by MDSCs is heterogeneous and requires more precise characterization in gastric cancer (GC) patients. Here, we have identified a novel subset of CD45+CD33lowCD11bdim MDSCs in the peripheral blood of GC patients compared to healthy individuals. CD45+CD33lowCD11bdim MDSCs morphologically resembled neutrophils and expressed high levels of the neutrophil marker CD66b. Circulating CD45+CD33lowCD11bdim MDSCs effectively suppressed CD8+ T cells activity through the inhibition of CD8+ T cell proliferation and interferon-γ (IFN-γ) and granzyme B (GrB) production. The proportion of CD45+CD33lowCD11bdim MDSCs also negatively correlated with the proportion of IFN-γ+CD8+ T cell in the peripheral blood of GC patients. GC patient serum-derived IL-6 and IL-8 activated and induced CD45+CD33lowCD11bdim MDSCs to express arginase I via the PI3K-AKT signaling pathway. This pathway contributed to CD8+ T cell suppression as it was partially rescued by the blockade of the IL-6/IL-8-arginase I axis. Peripheral blood CD45+CD33lowCD11bdim MDSCs, as well as IL-6, IL-8, and arginase I serum levels, positively correlated with GC progression and negatively correlated with overall patient survival. Altogether, our results highlight that a subset of neutrophilic CD45+CD33lowCD11bdim MDSCs is functionally immunosuppressive and activated via the IL-6/IL-8-arginase I axis in GC patients.

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The aim of the present study was to explore the potential role of cluster of differentiation CD68+ tumor-associated macrophages (TAMs) induced by interleukin (IL)-6 in the progression of gastric cancer (GC) and patient prognosis. The expression levels of IL-6 and CD68 were detected by immunohistochemical staining in 60 samples of tumor and non-tumor gastric tissues. CD14+ monocytes were isolated from peripheral blood mononuclear cells and stimulated with macrophage colony stimulation factor (M-CSF) and IL-6, and the expression levels of IL-10, IL-12, vascular endothelial growth factor (VEGF)-C and transforming growth factor (TGF)-ß were measured by reverse transcription polymerase chain reaction and ELISA. The GC MGC-803 cell line was co-cultured with monocytes stimulated by M-CSF and IL-6 and the invasion ability of the MGC-803 was evaluated by Transwell analysis. The levels of STAT3, P-STAT3 and interferon-regulatory factor 4 (IRF4) in the monocytes stimulated by M-CSF and IL-6 were detected by western blotting. The results demonstrated that the frequencies of IL-6+ macrophages (Mφs) and CD68+ Mφs were significantly higher in tumor regions compared with the corresponding non-tumor regions of GC tissues. Kaplan-Meier analysis revealed that the densities of tumor-infiltrating CD68+ or IL-6+ Mφs were inversely associated with the overall survival rates of the patients. In vitro, the expression levels of IL-10, VEGF-C and TGF-ß significantly increased in CD14+ monocytes subsequent to M-CSF and IL-6 stimulation. The invasion abilities of MGC-803 were increased by the monocytes stimulated with M-CSF and IL-6. The levels of STAT3, P-STAT3 and IRF4 proteins increased in the monocytes stimulated by M-CSF and IL-6. In conclusion, the results from the present study suggest that a high density of CD68+ TAMs predicts a poor prognosis in GC. IL-6 may polarize the Mφs and promote tumor invasion through the IL-6/STAT3/IRF4 signaling pathway.

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This study was aimed at the investigation of the effects of miR-21 on drug resistance, invasion, migration, and epithelial-mesenchymal transition (EMT) of lung adenocarcinoma cells and the related molecular mechanisms. Cell viability of A549 cell line was measured by MTT assay. Wound healing assay and transwell assay were, respectively, employed to examine cell migration and invasion abilities. The cells were transfected with miR-21 mimic or inhibitor using Lipofectamine 3000. The target relationship between miR-21 and HBP1 was confirmed by luciferase reporter gene assay. Western blot and qRT-PCR were used to examine the expression of HBP1 and EMT-related molecules. Compared with A549 cells, drug resistance of A549/PTX cells and A549/DDP cells were obviously stronger. A549/PTX cells and A549/DDP cells had stronger ability of migration and invasion compared with parental A549 cells. Meanwhile, EMT of A549/PTX and A549/DDP was significantly higher than that of A549 cells. MiR-21 promoted migration, invasion, and EMT of human lung adenocarcinoma cancer cells. Our experiment also verified the target relationship between miR-21 and HBP1. MiR-21 may affect migration and invasion ability of drug-resistant lung adenocarcinoma cells by targeting HBP1, therefore modulating EMT.

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The purpose of this study was to figure out the effect of ciRS-7/miR-7/NF-κB axis on the development of non-small cell lung cancer (NSCLC). In response, the expressions of ciRS-7, miR-7 and NF-κB subunit (ie RELA) within NSCLC tissues and cell lines were determined with real-time polymerase chain reaction (RT-PCR) and Western blot. Moreover, the NSCLC cells were transfected with pcDNA3-ciRS-7-ir, pcDNA3-ciRS-7, miR-NC and miR-7 mimic. Furthermore, the targeted relationships between ciRS-7 and miR-7, as well as between miR-7 and RELA, were confirmed by luciferase reporter assay. The proliferation, migration and apoptosis of NSCLC cells were, successively, measured using CCK-8 assay, wound-healing assay and flow cytometry test. Consequently, ciRS-7, miR-7, histopathological grade, lymph node metastasis and histopathological stage could independently predict the prognosis of patients with NSCLC (all P < .05). Moreover, remarkably up-regulated ciRS-7 and RELA expressions, as along with down-regulated miR-7 expressions, were found within NSCLC tissues and cells in comparison with normal ones (P < .05). Besides, overexpressed ciRS-7 and underexpressed miR-7 were correlated with increased proliferation, migration and invasion, yet reduced apoptosis rate of NSCLC cells (P < .05). More than that, ciRS-7 specifically targeted miR-7 to reduce its expressions (P < .05). Ultimately, the NSCLC cells within miR-7 + RELA group were observed with superior proliferative, migratory and invasive capabilities than those within miR-7 group (P < .05), and RELA expression was also significantly modified by both ciRS-7 and miR-7 (P < .05). In conclusion, the ciRS-7/miR-7/NF-kB axis could exert pronounced impacts on the proliferation, migration, invasion and apoptosis of NSCLC cells.

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Interleukin 6 (IL-6) was abundant in the tumor microenvironment and played potential roles in tumor progression. In our study, the expression of IL-6 in tumor tissues from 36 gastric cancer (GC) patients was significantly higher than in non-tumor tissues. Moreover, the number of CD163+CD206+ M2 macrophages that infiltrated in tumor tissues was significantly greater than those infiltrated in non-tumor tissues. The frequencies of M2 macrophages were positively correlated with the IL-6 expression in GC tumors. We also found that IL-6 could induce normal macrophages to differentiate into M2 macrophages with higher IL-10 and TGF-ß expression, and lower IL-12 expression, via activating STAT3 phosphorylation. Accordingly, knocking down STAT3 using small interfering RNA decreased the expression of M2 macrophages-related cytokines (IL-10 and TGF-ß). Furthermore, supernatants from IL-6-induced M2 macrophages promote GC cell proliferation and migration. Moreover, IL-6 production and CD163+CD206+ M2 macrophage infiltration in tumors were associated with disease progression and reduced GC patient survival. In conclusion, our data indicate that IL-6 induces M2 macrophage differentiation (IL-10highTGF-ßhighIL-12 p35low ) by activating STAT3 phosphorylation, and the IL-6-induced M2 macrophages exert a pro-tumor function by promoting GC cell proliferation and migration.

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BACKGROUND AND OBJECTIVE: Laparoscopy-assisted total gastrectomy (LATG) has not gained popularity due to the technical difficulty of esophagojejunostomy (EJ) and the high incidence of EJ-related complications. Herein, we compared two types of EJ for Roux-en-Y reconstruction to determine whether semi-end-to-end (SETE) EJ is more convenient than the end-to-side (ETS) procedure and is capable of reducing stricture and leakage. METHODS: A total of 268 patients who underwent LATG with Roux-en-Y reconstruction were included in this study. Two types of EJ were applied for LATG: conventional ETS EJ and SETE EJ. The surgical outcomes and postoperative complications were compared. RESULTS: The mean reconstruction time in the SETE group was shorter than that in the ETS group (41.6 ± 8.0 min vs 51.3 ± 9.2 min, P = 0.000). The incidences of total EJ-related complications, EJ leakage, and EJ stricture in the SETE group and ETS group were 1.1% (1/92) and 10.2% (18/176), 1.1% (1/92) and 4.0% (7/176), and 0 and 6.2% (11/176), respectively. The incidence of total EJ-related complications in the SETE group was lower than that of the ETS group (P = 0.006), and the incidence of EJ stricture in the SETE group was lower than that of the ETS group (P = 0.034). CONCLUSIONS: SETE EJ is more convenient than the conventional ETS procedure and is associated with a shorter reconstruction time and a lower incidence of EJ stricture and leakage.

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The deregulation of p53 in cancer cells is one of the important factors by which cancer cells escape from the immune surveillance. Cholecystokinin (CCK) has strong bioactivity in the regulation of a number of cell activities. This study tests a hypothesis that CCK interferes with p53 expression to affect the apoptotic process in lung cancer (tumor) cells. In this study, tumor-bearing mice and A549 cells (a tumor cell line) were irradiated. The expression of CCK and p53 in tumor cells was assessed with RT-qPCR and Western blotting. The binding of p300 to the promoter of p53 was evaluated by chromatin immunoprecipitation. We observed that, with a given amount and within a given period, small doses/more sessions of irradiation markedly increased the levels of CCK in the sera and tumor cells, which were positively correlated with the tumor growth in mice and negatively correlated with tumor cell apoptosis. CCK increased the levels of histone acetyltransferase p300 and repressed the levels of nuclear factor-kB at the p53 promoter locus in tumor cells, which suppressed the expression of p53. In conclusion, CCK plays an important role in attenuating the radiation-induced lung cancer cell apoptosis. CCK may be a novel therapeutic target in the treatment of lung cancers.

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OBJECTIVE: To compare video-assisted thoracoscopic surgery (VATS) lobectomy and conventional open lobectomy in patients with pulmonary tuberculosis (TB) who require surgery. METHODS: Forty patients with pulmonary TB who required lobectomy were randomized to receive either VATS or open lobectomy. Patient demographic, pulmonary function, operative, and postoperative data were compared between the groups. RESULTS: There were 20 patients who received VATS lobectomy (median age 31.5 years, range 19-67 years) and 20 that received open lobectomy (median age 33.5 years, range 16-60 years). The two groups were similar with respect to gender, age and pulmonary function (all, P>0.05). Lobectomy was completed by VATS in 19 of 20 patients (95%), and by thoracoscope-assisted mini-incision lobectomy in 1 patient. The median intraoperative blood loss was 345 mL (range, 100-800 mL), and the median duration of pleural cavity closed drainage was 5 days (range, 3-7 days). All open lobectomies were completed successfully, and the median intraoperative blood loss was 445 mL (range, 150-950 mL) and the median duration of pleural cavity closed drainage was 5 days (range, 3-9 days). No statistically significant differences were found between the groups with respect to operation completion rates, type of lung resection, intraoperative blood loss, closed pleural drainage duration and volume of postoperative chest drainage. The operation time, number of postoperative complications, postoperative pain index at 24 hours after surgery and postoperative hospital stay were all significantly less in the VATS group. With a median follow-up duration of 14 months (range, 8-18 months) no positive sputum examination results were found in either group. CONCLUSIONS: VATS lobectomy is an effective and minimally invasive method for treating patients with pulmonary TB.

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AIM: To test a new safe and simple technique for circular-stapled esophagojejunostomy in laparoscopic total gastrectomy (LATG). METHODS: We selected 26 patients with gastric cancer who underwent LATG and Roux-en-Y gastrointestinal reconstruction with semi-end-to-end esophagojejunal anastomosis. RESULTS: LATG with semi-end-to-end esophagojejunal anastomosis was successfully performed in all 26 patients. The average operation time was 257 ± 36 min, with an average anastomosis time of 51 ± 17 min and an average intraoperative blood loss of 88 ± 46 mL. The average postoperative hospital stay was 8 ± 3 d. There were no complications and no mortality in this series. CONCLUSION: The application of semi-end-to-end esophagojejunal anastomosis after LATG is a safe and feasible procedure, which can be easily performed and has a short operation time in terms of anastomosis.

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Circulating tumor cells (CTCs) from peripheral blood have been detected in most epithelial malignancies. CTCs are very heterogeneous and can be captured via different technologies based on their physical and biological properties. The detection rates have varied depending on the technology used for enumeration. Detection, monitoring, and molecular analysis of CTCs provide a powerful and noninvasive approach for the detection of early disease, assessing prognosis and therapeutic response in cancer patients. Non-small cell lung cancer (NSCLC) is one of the most lethal malignancies in humans. Compared with other solid tumors, the number of CTCs in NSCLC is relatively low. Nevertheless, NSCLC is a particularly important disease for CTC evaluation for prognostic purposes because of the lack of a reliable protein-based tumor marker. Molecular analyses of CTCs have provided new insights into the biology of metastasis with important implications for the clinical management of cancer patients. We review current and emerging technologies for CTC detection, with a focus on enrichment and molecular analysis of CTCs, and their potential clinical applications in NSCLC.

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OBJECTIVE: To explore the relationship between expressions of cell adhesion molecules CD44 v6 and E-cadherin (E-cad) and lymphatic metastasis in non-small cell lung cancer (NSCLC). MATERIALS AND METHODS: Eighty- seven tissue samples obtained from patients with primary NSCLC were collected in our hospital from Dec., 2007 to Dec., 2012, and the expressions of CD44 v6 and E-cad gene proteins in these samples were detected by immunohistochemical method. RESULTS: In the tissue without lymphatic metastasis, the positive expression rate of CD44 v6 was significantly lower, whereas the normal expression rate of E-cad was notably higher than that with lymphatic metastasis (55.6% vs. 78.4%, 47.2% vs. 21.6%), and both differences had statistical significance (P<0.05). Besides, CD44 v6 and E-cad expressions had a significant correlation in the NSCLC tissue with lymphatic metastasis (P<0.05). CONCLUSIONS: The positive expression of CD44 v6 and abnormal expression of E-cad may play a very important role in promoting lymphatic metastasis of NSCLC, with synergistic effect. Hence, detection of CD44 v6 and E-cad expressions is conductive to judging the lymphatic metastasis in NSCLC.

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